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level of alpha7 nAChR expression in the brain is critical for supporting the resistance to inflammatory and apoptogenic agents; the data presented may be a basis to create a new strategy for preventing and, possibly, slowing Alzheimer's disease development in humans
Varenicline promotes HUVEC migration by lowering VE-cadherin (show CDH5 ELISA Kits) expression due to activated ERK/p38 (show MAPK1 ELISA Kits)/JNK (show MAPK8 ELISA Kits) signaling through alpha7 nAChR. These processes probably contribute to varenicline-aggravated atherosclerotic plaque.
Comprehensive phenotyping revealed high prevalence of developmental delay/intellectual disability, autism spectrum disorder, and attention deficit/hyperactivity disorder in children with microduplications involving CHRNA7.
These results support our previous study showing that these PAMs are selective for the alpha7 AChR, and clarify that the procognitive/promnesic/antidepressant activity of PAM (show PAM ELISA Kits)-2 is not mediated by other targets.
Data (including data from studies conducted using knockout mice and SH-SY5Y cell line) suggest that Wnt/beta-catenin signaling is critical effector of CHRNA7-associated neuroprotection of dopaminergic neurons in substantia nigra; Parkinson's disease appears to develop without this neuroprotection.
Treatment of cells with nicotine induced the mRNA and protein levels of alpha7 nAChR; this could be abrogated by treatment with inhibitors targeting Src (show SRC ELISA Kits), PI3K (show PIK3CA ELISA Kits), MEK (show MAP2K1 ELISA Kits), alpha7 nAChR, CDK4/6 (show CDK4 ELISA Kits) or a disruptor of the Rb-Raf-1 (show RAF1 ELISA Kits) interaction.
Activation of alpha7nAChR alleviates Ang II (show AGT ELISA Kits)-induced vascular smooth muscle cell senescence by promoting NAD(+)-SIRT1 (show SIRT1 ELISA Kits) pathway.
the role of CHRNA4 (show CHRNA4 ELISA Kits) and CHRNA7 genetic polymorphisms in moderating auditory target and novelty attentional processing in healthy subjects exposed to the auditory "oddball" P300 (show EP300 ELISA Kits) paradigm.
We assume an additive effect of haploinsufficiency of ZBTB18 and CHRNA7 in our patient. Assembling the features of our patient and the published patients, we noted that only one of them showed mild anomalies of the corpus callosum.
results demonstrate the anti-inflammatory role of alpha7 nAChR in NK cells and suggest that modulation of its activity in these cells may constitute a novel target for regulation of the immune response.
Regulation of expression level and splicing of RIC-3 in brain and in immune cells following inflammation enables regulation of nicotinic acetylcholine receptor functional expression.
Data (including data from studies conducted using knockout mice and SH-SY5Y cell line) suggest that Wnt/beta-catenin signaling is critical effector of Chrna7-associated neuroprotection of dopaminergic neurons in substantia nigra; Parkinson's disease appears to develop without this neuroprotection.
Study compared the consequences of knocking out the alpha7nAChR on synaptic plasticity in C57/Bl6 and C3H mice, which differ in their basal alpha7nAChR expression levels; homozygous alpha7 deletion in C3H mice, which normally express higher alpha7nAChR levels, resulted in impaired long-term potentiation (LTP (show SCP2 ELISA Kits)) at hippocampal CA1 (show CA1 ELISA Kits) synapses, while C3H alpha7 heterozygous mice maintained robust LTP (show SCP2 ELISA Kits).
Activation of alpha7 nicotinic acetylcholine receptor on mast cells is a mechanism by which nicotine enhances atherosclerosis in ApoE (show APOE ELISA Kits) knockout mice.
We demonstrated that varenicline upregulates expression of LOX-1 (show OLR1 ELISA Kits) and CD36 (show CD36 ELISA Kits) significantly through alpha7 nAChR, thereby promoting oxLDL uptake in macrophages.
These data indicated that alpha7-nAChR caused the inhibition of ASPinduced activation of p38 (show CRK ELISA Kits) kinase and NFkappa B to inhibit the production of MCP1 (show CCL2 ELISA Kits) and keratinocytederived chemokine (show CCL1 ELISA Kits).
These results strongly suggest that activating alpha7nAChR can promote diabetic wound healing by suppressing advanced glycation end products-induced TNF-alpha (show TNF ELISA Kits) production, which may be closely associated with the blockage of NF-kappaB (show NFKB1 ELISA Kits) activation in macrophages.
It is concluded that inflammation decreases alpha7 nAChR expression in both mitochondria and cell plasma membrane and makes mitochondria more susceptible to apoptosis induction.
Results suggest that a nearly similar TBI-induced decrease in the alpha7 density in the brain of immature and adult animals is found, even with the differences in species, age and experimental procedures.
We conclude that residues in the M2 segment and flanking regions contribute to the unusual properties of the CHRNA7 receptor
Loop 3 and its docking to the alpha-helix is an important requirement for receptor assembly of the alpha7 nicotinic receptor.
a network of interactions formed by residues Lys (show LYZ ELISA Kits)-46, Asp (show ASIP ELISA Kits)-128, Asp (show ASIP ELISA Kits)-135, Asp (show ASIP ELISA Kits)-266, and possibly others appears to link agonist binding to channel gating
Lynx1 (show LYNX1 ELISA Kits) appears to act as a negative modulator of alpha7 nAChR-induced events by inhibiting Src (show SRC ELISA Kits) activation.
Chronic nicotine exposure up-regulates nAChR (show CHRNA4 ELISA Kits) activity in developing lung, and that nAChR (show CHRNA4 ELISA Kits) activity can be further modified by tyrosine phosphorylation.
The nicotinic acetylcholine receptors (nAChRs) are members of a superfamily of ligand-gated ion channels that mediate fast signal transmission at synapses. The nAChRs are thought to be hetero-pentamers composed of homologous subunits. The proposed structure for each subunit is a conserved N-terminal extracellular domain followed by three conserved transmembrane domains, a variable cytoplasmic loop, a fourth conserved transmembrane domain, and a short C-terminal extracellular region. The protein encoded by this gene forms a homo-oligomeric channel, displays marked permeability to calcium ions and is a major component of brain nicotinic receptors that are blocked by, and highly sensitive to, alpha-bungarotoxin. Once this receptor binds acetylcholine, it undergoes an extensive change in conformation that affects all subunits and leads to opening of an ion-conducting channel across the plasma membrane. This gene is located in a region identified as a major susceptibility locus for juvenile myoclonic epilepsy and a chromosomal location involved in the genetic transmission of schizophrenia. An evolutionarily recent partial duplication event in this region results in a hybrid containing sequence from this gene and a novel FAM7A gene. Alternative splicing results in multiple transcript variants.
a7 nicotinic acetylcholine receptor
, alpha 7 neuronal nicotinic acetylcholine receptor
, alpha-7 nicotinic cholinergic receptor subunit
, cholinergic receptor, nicotinic, alpha polypeptide 7
, neuronal acetylcholine receptor protein, alpha-7 chain
, neuronal acetylcholine receptor subunit alpha-7
, neuronal acetylcholine receptor subunit alpha-7-like
, cholinergic receptor, nicotinic, alpha 7
, acetylcholine receptor alpha 7 neural
, alpha7 nicotinic receptor
, C holinergic receptor nicotinic alpha polypeptide 7 (neuronal nicotinic acetycholine receptor alpha 7) (bungarotoxin alpha)
, C holinergic receptor, nicotinic, alpha polypeptide 7 (neuronal nicotinic acetycholine receptor alpha 7) (bungarotoxin alpha)
, bungarotoxin alpha
, neuronal nicotinic acetycholine receptor alpha 7
, nicotinic receptor alpha 7 subunit
, cholinergic receptor nicotinic alpha 7
, alpha 7 nicotinic acetylcholine receptor
, nicotinic acetylcholine receptor alpha7